Analysis of behavioral deficits produced by lesions in the dorsal and ventral midbrain tegmentum

Abstract

The impact of midbrain lesions on ingestive behavior in the rat was examined under a variety of pharmacological and dietary conditions. Electrolytic lesions in the dorsal midbrain tegmentum, ventrolateral to the central gray, produced moderate to severe (4 to 19 days) aphagia and adipsia in the rat. This effect was followed by complete recovery of ad lib food intake but a sustained suppression of water intake and urine output. Caloric regulation, drug-induced anorexia, drinking in response to intracellular and extracellular dehydration, and feeding as a function of dietary palatability appeared normal. Persistent deficits, however, were observed in the rats' feeding response to glucoprivation, in their consumption of sucrose or saccharin solutions, in post-fast compensatory food intake, and in their ability to maintain a nocturnal pattern of feeding. In contrast to these changes, electrolytic lesions in the ventral midbrain tegmentum produced an increase in food intake and body weight gain. This effect was associated with no other food- or water-related behavioral changes, with the exception of amphetamine- or mazindol-induced anorexia which was attenuated or abolished by the lesion.